Hormonal
Deficiency or inhibition of the nuclear receptor RORγ1 protects against diet-induced insulin resistance and improves glucose tolerance, potentially through mechanisms distinct from RORα.
This research suggests that modulating RORγ1 activity could be a strategy to improve insulin sensitivity. The paper notes that RORγ1 expression positively correlates with adipocyte size and insulin resistance in humans, implying that inhibiting this receptor might help manage type 2 diabetes risk.
Deficiency in RORγ also protects against diet-induced insulin resistance by a mechanism that appears different from that in RORα deficiency... In obese RORγ −/− mice... Fasting blood insulin levels were shown to be significantly lower... and mice displayed improved insulin sensitivity.
Why this rating
Evidence is derived from mouse models (RORγ-deficient) and human observational studies correlating RORγ1 expression with adipocyte size and insulin resistance.
Source
Retinoic acid-related orphan receptors α and γ: key regulators of lipid/glucose metabolism, inflammation, and insulin sensitivity
Anton M. Jetten et al. · Frontiers in Endocrinology · 2013
DOI 10.3389/fendo.2013.00001
More from this paper
- Deficiency or inhibition of the nuclear receptor RORα protects against diet- and age-induced obesity, hepatosteatosis, and insulin resistance by increasing energy expenditure and suppressing pro-inflammatory gene expression in adipose tissue.Moderate
- RORs (RORα and RORγ) function as intermediaries linking the circadian clock machinery to the regulation of lipid and glucose metabolism, suggesting that circadian disruption may contribute to metabolic syndrome.Moderate
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